Evidence map›Paper›PMID 32728764›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

IL-33 deficiency protects mice from DSS-induced experimental colitis by suppressing ILC2 and Th17 cell responses.

Xueying Qiu, Chang Qi, Xiaoxiao Li, Dai Fang, Min Fang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Emerging Effects of IL-33 on COVID-19.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Xueying QiuDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13# Hangkong Road, Wuhan, 430030, China.
Chang QiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13# Hangkong Road, Wuhan, 430030, China.
Xiaoxiao LiDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13# Hangkong Road, Wuhan, 430030, China.
Dai FangDepartment of Biostatistics, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Min FangDepartment of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13# Hangkong Road, Wuhan, 430030, China. minfang89@hust.edu.cn.ORCID http://orcid.org/0000-0002-1835-5702
Huazhong University of Science and Technology · CNRutgers, The State University of New Jersey · US

Funding

National Natural Science Foundation of China 81373167National Natural Science Foundation of China 91542110
6 · The paper itself

Abstract

backgroundRecently, IL-33-driven ILC2 response has been shown to participate in a variety of diseases. However, IL-33-driven ILC2 immunity has not been extensively characterized in the context of colitis yet. MATERIALS AND SUBJECTS: The RAG-2- and IL-33-deficient mice were used to investigate the role and underlying mechanisms of IL-33-driven ILC2 response in the DSS-induced experimental colitis. Body weight, length of colon, and histological analysis were monitored to evaluate the severity of colitis. Proportions of immune cells were examined by flow cytometry. Levels of cytokines were analyzed by ELISA and q-PCR.

resultsAdministration of exogenous IL-33 aggravated the DSS-induced colitis, which revealed that IL-33 promoted the generation of ILC2 cells to mediate the inflammation of colon. Consistently, this effect was confirmed in RAG-2-deficient mice without T, B cells. Furthermore, IL-33-deficient mice were used to examine the role of endogenous IL-33 on the pathogenesis of DSS-induced colitis. Interestingly, lack of endogenous IL-33 protected the mice from the DSS-induced colitis. The protective effect is associated with impairments of development of ILC2 as well as Th17 cells. Analysis of their cytokine production profiles revealed that IL-33 deficiency resulted in the reduction of cytokines IL-6 and IL-1β as well as IL-10. These results suggest that IL-33/ILC2 axis is a potential therapeutic target for human colitis.

conclusionOur findings demonstrate that IL-33 deficiency protects mice from DSS-induced colitis. The protective effect is associated with impairments of ILC2 and Th17 cell development as well as reduction of inflammatory cytokines IL-6 and IL-1β.

Indexed as

AnimalsColitisColonCytokinesDendritic CellsDextran SulfateDisease Models, AnimalDNA-Binding ProteinsImmunity, InnateLymphocytesMaleMice, Inbred C57BLMice, KnockoutCytokinesDextran SulfateDNA-Binding ProteinsRag2 protein, mouseColitisDSS (dextran sulfate sodium)Group 2 innate lymphoid cellsInterleukin (IL)-33Th17 cells

Identifiers

PMID32728764
OpenAlexW3045860244

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.